Abstract TMP54: Carotid Artery Inflammation Following Air Pollution Exposure

Abstract

Background: The hallmark of inflammation is activation of the immune system, recruitment of leukocytes and induction of proinflammatory cytokines. Air pollution induced nano-size particulate matter (nPM) from vehicular exhaust is a potent environmental source of inflammation. The carotid arteries, a principle source of blood flow to the brain, are susceptible to inflammatory changes. Objective: To examine the effects of nano-size particulate matter (nPM) exposure on vascular tissue inflammation in the common carotid artery in mice. Methods: Particulate Matter was collected from an urban area in central Los Angeles, transferred to aqueous suspension by vortexing and sonication and reaerosolized for animal exposure. Mice were exposed to filtered air (n=7) or nPM (n=7) for a duration of 10 weeks, 3 days a week for 5 hours. Following the exposure period, animals were sacrificed and common carotid arteries were extracted, frozen, cut axially at 20um, and mounted on slides. Immunohistochemical analysis was performed. Staining was analyzed for presence of Intercellular Adhesion Molecule 1 (ICAM-1), endothelial surface adhesion molecule activated by leukocytes, and leukocyte antigen 6G precursor (Ly6g), a maker for monocytes and neutrophils. Results: An average of 5 axial sections were taken from carotid arteries of 14 mice (Filter n=7, nPM =7). Mean ICAM-1 values were computed for each carotid artery. Group averages were compared between cohorts of mice exposed to filtered air and nPM. Semiquantitative immunohistochemical analysis of the intimal and medial layers of the common carotid arteries demonstrated increased ICAM-1 in mice exposed to nPM (filter 15.6 SD +/-1.7 vs nPM 19.7 SD +/-3.4, p=0.01), but did not demonstrate differences in Ly6g values (filter mean 19.4, SD +/-3.9 vs nPM mean 16.1, SD +/-2.7, p=0.1) Conclusion: Higher ICAM-1 concentrations on carotid arteries exposed to nano-size particulate matter indicates inflammatory upregulation of adhesion molecules. However, there is no clear increase in circulating leucocytes within the vessel wall.